Atrial fibrillation is associated with brain lesions indicating silent cerebral ischemia, similar to its link with symptomatic stroke, a study showed.

Action Points

Note that this cross-sectional study of patients presenting to a cardiovascular disease prevention clinic demonstrated that the vast majority of patients with atrial fibrillation had evidence of silent cerebral ischemia on MRI.

Be aware that many lesions appeared to be embolic in nature.

Atrial fibrillation (Afib) is associated with brain lesions indicating silent cerebral ischemia, similar to its link with symptomatic stroke, a study showed.

The arrhythmia correlated with 7.2-fold higher risk of having at least one silent stroke apparent on MRI after controlling for age, stroke risk score, and anticoagulant treatment (P=0.001), Fiorenzo Gaita, MD, of the University of Turin, Italy, and colleagues found.

But the lesions didn't appear entirely benign for these patients with no prior clinically-apparent stroke, the group reported online in the Journal of the American College of Cardiology.

Cognitive performance was significantly worse with persistent or paroxysmal Afib than with sinus rhythm. Scores averaged 83, 86, and 92 points, respectively, on the Repeatable Battery for the Assessment of Neuropsychological Status (P<0.01), which the researchers called a "relevant clinical shift" from medium to medium-low function.

These findings are important in confirming yet another way Afib can damage the brain, atop the well-established link with stroke and transient ischemic attack, commented Steven Shea, MD, and Marco Di Tullio, MD, both of Columbia University Medical Center in New York City.

Now "the most important question is whether prophylactic antithrombotic treatment may be able to reduce the incidence of silent brain lesions as it has been proven to do for clinical strokes," they wrote in an accompanying editorial.

The study didn't have an adequate measure of exposure to antithrombotic agents during Afib episodes, ruling out conclusions regarding treatment effect. Shea and Di Tullio called for appropriately designed and powered prospective studies to look at that issue.

Gaita's study included 270 individuals screened from consecutive patients presenting to a cardiology or cardiovascular prevention clinic at a single center to generate age, gender, risk factor, and education balanced groups -- 90 with paroxysmal Afib, 90 with persistent Afib, and 90 controls in sinus rhythm.

MRI indicated silent cerebral ischemia lesions in 89% patients with paroxysmal Afib and 92% with persistent Afib compared with 46% of controls, which wasn't significantly different between the two types of Afib but was for both versus controls (P<0.01).

The number of these lesions averaged 41 in persistent Afib, 33 in paroxysmal Afib, and 12 in controls, which was significantly different for all three groups.

The high prevalence of these lesions in the control group compared with what has been reported in the general population may have reflected the moderate to high cardiovascular risk among these patients referred for cardiovascular prevention or treatment, the researchers suggested.

The lesions can have either ischemic and embolic origins, but the peculiar "spotted" distribution of "small sharply demarcated lesions, often in cluster, with bilateral distribution, prevalently in the frontal lobe" seen in 50% and 67% of the paroxysmal and persistent Afib patients, respectively, strongly supported an embolic mechanism, they noted.

Limitations of the study included the cross-sectional design and the limited set of cognitive functions measured in the study.

The editorialists also brought up the possibility of mislabeling of Afib, which was clinically defined and might have missed asymptomatic arrhythmia.

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